The Impact of Catastrophization and Emotions on Pain: A Narrative Review of Underlying Mechanisms

Abstract

Pain is a common experience that can lead to poor physical, cognitive, and social function when it becomes chronic. Although the development of the biopsychosocial model of pain improved recognition that biologic factors alone are not enough to explain the experience of pain, psychosocial and lifestyle interventions remain underutilized. Two psychosocial constructs that have implications for pain perception are catastrophization and emotions. The objective of this narrative review was to examine the current understanding of the mechanisms by which catastrophization and emotions modulate pain. We found that key shared mechanisms of catastrophization and negative emotions were increases in HPA axis and sympathetic activity, which promote pain sensitivity. Additionally, both constructs interfered with endogenous opioids, leading to diminished pain resistance. Catastrophization differed from negative emotions in that it involved greater connectivity of the salience network with the default mode network, leading to increased attention to pain. In contrast, positive emotions were associated with much of an opposite effect with increases in parasympathetic activity and endogenous opioid release, which reduce pain intensity. Specific interventions that may be effective in blunting the mechanisms underlying the negative impacts of catastrophization and emotions include mindfulness and relaxation exercises, cognitive behavioral therapy, and yoga. Possible changes to the workflow suggested by our findings include better assessment of coping abilities and strategies at baseline, identifying individuals at risk of catastrophizing, and using contextual factors, such as a greater focus on positive outcomes.

Introduction

Pain is extremely common, accounting for over 40% of Emergency Department visits.¹ It can negatively impact several aspects of a person’s life, especially when it becomes chronic and maladaptive. Higher intensity pain generally results in worse outcomes, including poorer physical function and quality of life.^2,3 Higher rates of substance abuse, divorce, and suicide have also been observed among individuals with chronic pain.⁴ Cognitively, chronic pain has been linked to reduced working memory.⁵ Individuals may also experience decreased work ability due to various factors, including pain interference and poor function.^6,7 The reduced ability to work and increased healthcare utilization have resulted in total annual costs of approximately $560 billion in the United States.⁸

Adequate control of pain and pain-related burden remains a challenge, leaving many patients dissatisfied.⁹ Part of the problem may stem from historical context. Before the mid-20^th century, pain was viewed as a strictly biological process.¹⁰ During this time, however, clinicians questioned how the biomedical model could explain differences in pain presentation (eg., pain intensity) and treatment response across patients with the same diagnosis.¹¹ Furthermore, the impact of pain on physical function and other quality-of-life metrics varies significantly among individuals with identical conditions. This led to the introduction of the biopsychosocial model, which emphasizes a more holistic approach to the patient, recognizing pain as a unique experience rather than a simple symptom.⁴ Many of the contributory factors implicated in this model (eg., anxiety and sleep) are also consequences of chronic pain itself, leading to a positive feedback loop that further fuels the manifestation of pain. Despite the development of this model, the routine incorporation of psychosocial and lifestyle interventions into clinical practice for chronic pain management is still sparse.¹²

One possible reason why psychosocial factors have not been addressed in a widespread manner may be due to a limited understanding of how these factors influence pain. Catastrophization and emotions are two context-dependent processes that can induce nocebo effects but have unclear mechanisms. A better understanding of underlying mechanisms may help guide future treatment strategies to optimize patient outcomes. This narrative review aims to describe the mechanisms by which catastrophization and emotions contribute to the experience of pain.

Methodology

This narrative review was conducted using a PubMed literature search for relevant articles published from inception through October 2025. Keywords searched include terms and synonyms for “catastrophization”, “catastrophizing”, “emotion”, and “pain”. Both reviews and original research studies (human or animal design) were eligible for inclusion. Articles were included if they contained content pertaining to physiologic/biologic effects of catastrophization and emotions in relation to pain. Articles were excluded if they were not published in the English language or were not peer reviewed.

Overview of Pain Signaling Pathways

Pain signaling initiates when nociceptors in the dermis and/or epidermis are stimulated.¹³ Stimulation of nociceptors results in the signal traveling to the dorsal root ganglion via afferent Aδ and C fibers. From there, the signal travels from the peripheral nervous system to the central nervous system, passing through the dorsal horn of the spinal cord, where the first synapse occurs. Following this synapse, pain signaling decussates and travels up the spinal cord via the lateral spinothalamic tract (sensory-discriminative pathway) and spinoreticular tracts (affective pathway). Pain signals ascending the spinothalamic tract travel to the thalamus, where the second synapse occurs at the ventral posterior lateral nucleus, before being relayed to the primary somatosensory cortex, alerting the person that they are experiencing pain via the third and final synapse. Signals in the spinoreticular tracts travel to various regions of the brainstem (eg., periaqueductal grey [PAG]) and brain (eg., limbic system) to modulate the autonomic nervous system. The spinoreticular tract’s signaling and subsequent effects may form the basis for how psychological processes, such as catastrophizing and emotions, may influence pain responses.^14,15

Mechanisms of Catastrophization and Its Relationship to Pain

While many studies have demonstrated the link between catastrophization, pain intensity, and adverse clinical outcomes, the precise mechanism remains elusive, making a consistent definition of the construct challenging. Contemporary research conceptualizes catastrophization within several complementary explanatory frameworks. The earliest and most influential is the cognitive-behavioral model, which describes the process of catastrophization as the result of maladaptive cognitive appraisals and interpretive biases that exaggerate the threat of pain and underestimates one’s ability to cope.¹⁶ In contrast, the communal coping model describes catastrophization as a social-communicative behavior, potentially explaining why it occurs. This model posits that individuals exhibit exaggerated expressions of distress, verbally or non-verbally, to elicit support from others and thus indirectly regulate negative affect. More recently, catastrophization has been investigated as a trait-like disposition, reflecting stable differences in threat sensitivity and negative affectivity that may extend beyond the context of pain. Although the trait model suggests there may be overlap with general emotional vulnerability, catastrophization remains a distinct construct that can be independently addressed.¹⁷

Cognitive Model

From a cognitive-behavioral perspective, catastrophization is seen as a maladaptive appraisal process that exaggerates the threat value or expectation of pain.¹⁸ A cue of pain naturally demands attention from the brain, both consciously and subconsciously, to evaluate and solve this potential crisis. Catastrophization occurs when the individual overestimates the harm of the pain and underestimates their ability to cope, brought about by automatic cognitive errors.¹⁹ Among the three core components of catastrophization (magnification, rumination, and helplessness), the perception of low self-efficacy or inability to cope often initiates this cognitive cascade.²⁰

Individuals who demonstrate an inability to cope show greater attentional focus on pain cues and higher rumination over the potential consequences of pain.²¹ Several studies have explored the connection between the individual beliefs regarding their ability to cope with pain and pain intensity. One study looking at 430 patients with chronic pain found a significant correlation between self-efficacy, pain intensity, and pain catastrophizing, which held even after adjustment for covariates such as age, gender, clinical symptoms, and socioeconomic status.²² Notably, the observed relationship between reported pain intensity and catastrophization was partially mediated by chronic pain self-efficacy. This mediator role has also been observed in the context of acute pain, including post-abdominal surgery pain.²³ The results of these studies support the mechanistic importance of cognitive evaluations regarding pain in catastrophization and the role of patient beliefs in determining pain outcomes.

Furthermore, catastrophization has been understood as a result of a maladaptive pain schema, which is defined as a hierarchically organized knowledge structure that integrates past experiences, threat expectations, and beliefs about personal control.²⁴ While schemas typically facilitate the navigation of complex sensory inputs and adaptive responses, they can become distorted by repeated threat-biased appraisals, leading to a threat-dominant, control-deficient representation. When activated, it biases both appraisal and attention toward pain-related cues, impairing disengagement and reinforcing misappraisal of pain as an inevitable or intolerable outcome. Priming studies, which use subtle activation of a cognitive schema to observe its impact on subsequent behavior, have demonstrated that verbal cues with semantic association to pain are associated with changes in both catastrophization and reported pain intensity.^25,26 These experimental findings provide evidence for the cognitive model and the theory that catastrophization is driven by distortions of a pre-existing pain representation that automatically emerges outside of conscious awareness.

Coping Model

Like most forms of human cognition and behavior, catastrophization may be shaped by social context and external feedback. The communal coping model theorizes that catastrophization is not a means of directly managing pain but a communicative coping strategy to elicit empathy and support from one’s social network.¹⁹ Verbal and non-verbal expressions of distress serve to externalize fear, often producing reassurance and care from significant others. Such positive responses can temporarily reduce distress and enhance perceived social support and connection, functioning as a short-term coping tool. Higher levels of catastrophization have been associated with both increased seeking of support from partners and a perception of higher pain intensity by external observers.²⁷

Over time, this strategy can become maladaptive, causing increased relationship strain and worsened pain. Studies comparing acute and chronic pain populations show that while brief catastrophization episodes often evoke empathy and reassurance, chronic expressions can erode partner relationships and predict lower perceived spousal support.^28,29 Interestingly, higher levels of catastrophization are associated with increased perceived spousal hostility and support, suggesting that even well-intentioned or sympathetic responses may contain subtle feedback that patients can construe as criticism.³⁰ Furthermore, the relationship can be bidirectional, as catastrophization has been associated with increased negative affect for spouses, while negative or punishing responses, in turn, reinforce catastrophic thinking and worsen perceived pain.³¹ Conversely, some have proposed that supportive reactions may reinforce catastrophization by rewarding individuals for exaggerated expressions of pain and fear, thereby maintaining the behavior through social learning.²⁹ However, empirical evidence for positive reinforcement as a primary driver of catastrophization remains limited.

Trait Model

Contrary to earlier models, the trait or dispositional model conceptualizes catastrophization as a relatively enduring cognitive-affective tendency rather than a transient maladaptation specific to painful experiences. It posits that individuals differ consistently in their propensity to magnify, ruminate, and feel helpless about pain.¹⁶ To this point, catastrophization is relatively stable in the absence of interventions and has been closely linked to personality traits such as neuroticism. One retrospective study of 595 patients with non-malignant chronic pain found that neuroticism was independently associated with greater pain catastrophizing across varying levels of depression.³² In a separate experimental study of 1322 healthy individuals, pain catastrophizing was observed to serve a mediating role in the relationship between neuroticism and intensity of induced pain.³³

Twin studies suggest the existence of a significant genetic component to pain catastrophizing. In a study of 206 monozygotic and 194 dizygotic twins, researchers used a cold-pressor task to examine catastrophization and pain responses, finding that genetic factors accounted for 37% of the variance in catastrophization.³⁴ Recent genetics studies have also identified specific polymorphisms that may be associated with pain catastrophizing.³⁵ While the molecular mechanisms underlying such genetic processes remain elusive, these findings imply that catastrophization is partially explained by biologically grounded factors that influence affective predispositions.

Nonetheless, catastrophization demonstrates contextual fluctuations and modifiability through experimental interventions. This suggests that the influence of dispositional tendencies is complex and not entirely separable from situational appraisals, making it challenging for the individual to evaluate objectively. To this point, researchers have argued that current methods for quantifying catastrophization via self-report capture broader constructs of negative affectivity, such as worrying and fear, rather than a distinct pain-catastrophizing axis.³⁶ Therefore, while catastrophization is strongly associated with certain personality traits, a more person-centered, longitudinal approach may be required to delineate whether it is a unique cross-situational trait.

Implications of the Three Models of Catastrophization

These complementary models describe different aspects of catastrophization and may provide insights for future therapeutic interventions and preventative measures (Table 1). According to the cognitive model, maladaptive thought processes are a major component of catastrophizing.^16,18 To alter these processes, it may be important to implement psychosocial interventions such as Cognitive Behavioral Therapy or Cognitive Bias Modification of Interpretations in patients who are actively catastrophizing or at risk.^37,38 Based on the trait model, some individuals are more likely to catastrophize and may require early psychosocial intervention.¹⁶ To identify those at greater risk of catastrophizing, questionnaires can be administered that assess the tendency to catastrophize (eg., Pain Catastrophizing Scale) or personality traits associated with negative affectivity (eg., Neuroticism Scale).^39,40 Lastly, the coping model describes catastrophization as a short-term coping strategy.¹⁹ This may suggest that more attention should be placed early in assessing people’s coping abilities and how they cope. Individuals with a history of poor coping or social coping may benefit from switching to a more problem-focused approach, such as active coping.⁴¹

Table 1.

Summary of the Three Models of Catastrophization and Their Implications

Model	Aspect Described	Findings	Implications
Cognitive	What happens during catastrophization?	Catastrophization involves maladaptive cognitive appraisals and interpretive biases leading to: Increased attention to pain Overestimation of pain Underestimation of coping abilities Poor self-efficacy	Integrate psychosocial interventions into pain management
Coping	Why does catastrophization occur?	Catastrophization may be used as a short-term coping strategy to externalize distress and gain social support or reassurance Long-term use of catastrophization as a coping strategy can negatively impact relationships and be detrimental for pain	Assess individual coping strategies and abilities
Trait	Who is more likely to catastrophize?	Individuals with negative affectivity, specifically neuroticism, are more prone to catastrophizing Genetics may have some impact in tendencies to catastrophize, but evidence remains limited	Identify individuals more likely to catastrophize with questionnaires

Physiologic Mechanisms

The physiologic mechanisms associated with catastrophization are fascinating, as they elucidate how cognitive-affective processes translate into somatic pain amplification and poor clinical outcomes. Catastrophization has been theorized to worsen pain in some diseases through its association with increased muscle tension, autonomic arousal, and hypothalamic-pituitary-adrenal (HPA) axis activation, thereby sustaining physiological stress responses that exacerbate chronic disease states (Table 2).^42,43

Table 2.

Mechanisms of Pain Catastrophization

Physiologic Mechanisms	Neural Mechanisms
Overactivation of sympathetic nervous system and diminished parasympathetic activity Hypothalamic-pituitary-adrenal axis activation Reduced endogenous opioid function	Increased activity in: Anterior cingulate cortex Insula Thalamus Primary and secondary somatosensory cortices Decreased activity in: Dorsolateral prefrontal cortex Increased connectivity between the salience network (ACC and insula) and posterior cingulate cortex (default mode network)

Autonomic reactivity is among the clearest physiological correlates of catastrophization. In experimental studies, individuals who catastrophize more often exhibit higher heart rate and skin conductance responses, which suggests sympathetic overactivation and reduced parasympathetic modulation.⁴⁴ One study found that catastrophization and pain intensity were associated with increased heart rate during a cold-pressor task, without similar psychosocial associations with systolic and diastolic blood pressure changes, suggesting selective autonomic activation rather than generalized cardiovascular strain.⁴⁵

Furthermore, catastrophization appears to influence endocrine responses to stress. A study of salivary cortisol in patients with temporomandibular joint disorder found that higher catastrophization scores were associated with elevated cortisol levels, indicating sustained HPA axis activation and a flattened cortisol recovery response.⁴⁶ Chronic activation of this system may contribute to the poor functional outcomes, such as fatigue and hypervigilance to pain, observed in catastrophizing patients. In addition, catastrophization has also been associated with reduced endogenous opioid function, suggesting impaired pain inhibition.⁴⁷ The results from these studies suggest that catastrophization is accompanied by a consistently observable pattern of physiological dysregulation, possibly contributing to increased pain perception and persistence of pain-related distress. However, it is important to note that much of this current evidence from human studies involves experimental pain models, which may not be directly applicable to the general chronic pain population, as participants in these models may often perceive the pain as temporary and controlled. Small sample sizes within these studies also limit the strength of evidence.

Neural Correlates

Neuroimaging studies have provided important insights into the neural pathways underlying catastrophization of pain, revealing significant overlaps with those involved in pain perception and modulation (Table 2). These studies quantified catastrophization using the Pain Catastrophizing Scale or Coping Strategies Questionnaire and used fMRI to visualize brain activity during tasks that invoked pain.^48–50 Such tasks included experimental pain models (eg, mechanical, thermal, or electrical stimuli) and movements that aggravated existing chronic pain conditions. Across fMRI studies, key brain regions associated with differences in activity during painful stimuli in patients with higher catastrophization scores include the anterior cingulate cortex (ACC), insula, thalamus, primary and secondary somatosensory cortices, and dorsolateral prefrontal cortex. These structures also serve as core regions for pain processing, affective evaluation, and top-down control, processes that may also be implicated in pain catastrophization.

Functional connectivity analyses using advanced MRI techniques, including diffusion tensor imaging and resting-state fMRI, have allowed researchers to investigate how catastrophizing influences the functional organization of brain networks. Several studies have found increased connectivity between the salience network (ACC and insula) and the posterior cingulate cortex node of the default mode network (DMN) during pain anticipation and pain experience in individuals with high levels of catastrophization.^51,52 The DMN primarily involves self-referential thought and remains active during rest or in the absence of external task engagement. In contrast, the salience network detects and prioritizes emotional or physiologic stimuli and recruits other functional networks. Hyperconnectivity between these networks may signal increased integration of threat signals within self-focused evaluation processes, providing a neurophysiologic explanation for the heightened attentional engagement and pain perception observed during catastrophization.

Mechanisms of Emotion and Its Relationship to Pain

Similar to catastrophization, emotional stress influences pain perception through mixed neuroimmune and endocrine pathways (Table 3). Negative emotions such as anger and sadness are associated with impairment of pain-inhibitory processes. Reduced dopaminergic tone observed in depression or chronic stress diminishes opioid signaling and weakens pain inhibition.^53,54 Negative affect is also linked to increased amygdala activation, which increases facilitatory signaling to the PAG and RVM, diminishing inhibitory control and enhancing pain sensitivity.⁵⁵ This amygdala excitation is partly mediated by corticotropin-releasing hormone (CRH) projections that shift PAG-RVM output from inhibitory to facilitatory, promoting hyperalgesia. Simultaneously, weakened prefrontal regulation fails to suppress limbic overactivation, which amplifies emotional distress and pain perception.⁵⁶ Negative emotional states are associated with hyperactivity of limbic responses, reduced parasympathetic tone, increased sympathetic arousal, and amplified nociceptive transmission; these factors collectively contribute to lower pain thresholds and prolonged discomfort.⁵⁷

Table 3.

Key Mechanisms of Negative versus Positive Emotions and Pain

Negative Emotions	Positive Emotions
Reduced dopaminergic signaling → diminished endogenous opioid release Weakened prefrontal regulation → limbic overactivation Activation of the hypothalamic-pituitary-adrenal axis and sympathetic nervous system → release of proinflammatory cytokines	Increased dopaminergic signaling → enhanced endogenous opioid release Increased connectivity between the anterior cingulate cortex and periaqueductal gray Increased parasympathetic tone and reduced sympathetic activity
Overall effect = elevated pain sensitivity, diminished pain inhibition	Overall effect = reduced pain sensitivity, enhanced pain inhibition

Emotional stress is associated with activation of the HPA axis and the sympathetic nervous system, leading to the release of cortisol and catecholamines. Over time, prolonged activation of the HPA axis and sympathetic nervous system disrupts the immune balance, leading to adverse health effects. In individuals with depression, this dysregulation has been found to result in increased concentrations of pro-inflammatory cytokines such as interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), which sensitize nociceptive neurons and enhance central pain processing.⁵⁸ On a molecular level, IL-1β and TNF-α enhance transmission of excitatory molecules, while IL-6 decreases inhibitory signaling in dorsal horn neurons.

In animal models, increased excitatory and decreased inhibitory signaling leads to central sensitization mediated by CREB phosphorylation and transcription of pro-nociceptive genes, including COX-2 and somatostatin.⁵⁹ These pro-inflammatory cytokines can cross the blood-brain barrier and influence glial activity, releasing additional inflammatory cytokines and reactive oxygen species, which amplify neuroinflammatory signaling.⁶⁰ These glial cytokines suppress inhibitory networks and enhance glutamatergic excitability, leading to disrupted neurotransmission, synaptic loss, and increased pain sensitivity. Clinically, people with major depressive disorder often exhibit elevated IL-6 levels, which enhance neuroinflammation and glial activation that directly contribute to allodynia and hyperalgesia.⁶¹ Similarly, IL-1β alters neuronal excitability and disrupts monoamine transmission, particularly in the serotonergic and dopaminergic pathways, linking affective dysregulation to increased pain signaling.⁶²

Chronic anxiety and emotional stress have been observed to prolong the inflammatory response in both human and animal models by blunting glucocorticoid receptor (GR) sensitivity, ultimately resulting in cortisol resistance and impaired feedback inhibition of the HPA axis.⁶³ GR resistance arises from reduced GR nuclear translocation, increased GRβ isoform expression, and NF-κB-mediated suppression of GR transcriptional activity. This molecular impairment weakens cortisol’s anti-inflammatory effects, allowing persistent cytokinemia and sustained activation of stress-related transcription factors. Consequently, IL-6 and TNF-α remain elevated, maintaining a pro-inflammatory state linked to chronic pain. This dysregulation hinders the inflammatory response from subsiding and reinforces pain sensory pathways.⁶⁴ Additionally, stress and anxiety suppress vagal tone and the cholinergic anti-inflammatory reflex, which further facilitates peripheral and central inflammation.⁶⁵ Cytokine-driven inflammatory changes modulate pain signaling, impair neuroplasticity and mood regulation, and establish a common biological pathway linking inflammation, pain, and negative affect. This interconnection sustains a feedback loop in which emotional stress amplifies inflammatory activity, and, in turn, inflammation exacerbates both pain perception and emotional distress.⁶⁶ Therefore, emotions and psychiatric disorders may heighten pain through their association with the activation of pro-inflammatory mechanisms, primarily via IL-1β and IL-6, which bridge immune signaling, neuroendocrine stress responses, and central pain sensitization.

Emotion and nociception interact through shared neural networks mediating pain and emotional experience. The ACC integrates information related to motivation, affect, and action, coordinating emotional and behavioral responses to pain.⁶⁷ In particular, the rostral and dorsal regions of the ACC play a critical role in processing the affective aspect of pain. Similarly, the insula serves as an integrative hub where interoceptive, emotional, and sensory inputs converge, and neurons responsive to pain and aversive stimuli project to the thalamus and amygdala, linking emotional experience with nociceptive processing.^68,69 Hence, these structures demonstrate that the emotional regulation of pain is a biologically grounded process involving reciprocal feedback among cortical, limbic, and brainstem circuits.

What About Positive Emotions?

Positive emotions may contribute to reduced pain perception and processing, largely by enhancing endogenous inhibition pathways (Table 3). In experimental studies of conditioned pain modulation (CPM), individuals who experienced happiness showed more potent descending inhibition and reported reduced pain intensity than those who experienced negative emotions.⁷⁰ This observation supports previous findings that a positive emotional state is linked to reduced pain intensity, possibly through improving one’s coping ability by diverting attention away from the pain.⁷¹ Positive emotions are involved in reward and motivation neural pathways, which may modulate descending inhibitory circuits and facilitate the release of endogenous opioids that suppress nociceptive signaling.

The endogenous pain control mechanism associated with positive affect functions via interconnected cortical, limbic, and brainstem structures that regulate nociceptive input through top-down modulation. Key components of this mechanism include the PAG in the midbrain, rostral ventromedial medulla (RVM), and locus coeruleus (LC). These nuclei have distinct neurochemical roles; projections from the RVM inhibit nociceptive neurons through serotonin receptors, while noradrenergic output from the LC acts via α₂-adrenoceptors to silence dorsal horn excitatory neurons.^72,73 Endogenous opioids, such as β-endorphins and enkephalins, modulate the PAG and RVM networks via μ- and δ-opioid receptors, thereby suppressing ascending nociceptive transmission.⁷⁴ These nuclei form the core of the descending inhibitory system that projects to the spinal dorsal horn, where inhibitory neurotransmitters like serotonin, norepinephrine, and opioids attenuate nociceptive transmission. The PAG integrates emotional and cognitive information from higher brain regions, including the ACC, prefrontal cortex, amygdala, and hypothalamus. It acts as a hub that links emotional states to pain modulation. Activation of the PAG triggers opioid-mediated inhibitory output to the RVM, which in turn modulates spinal pain processing through descending serotonergic pathways. Similarly, noradrenergic projections from the LC amplify inhibition of nociceptive neurons in the dorsal horn and contribute to the analgesic effects associated with positive affective states.⁷⁵

The neurochemical and physiological effects associated with positive emotion further support the enhanced engagement of the descending modulatory networks. Positive mood states correlate with enhanced dopaminergic signaling in the ventral tegmental area (VTA) and nucleus accumbens, linking reward-related neural circuits with the PAG-RVM descending pain-modulatory pathway to facilitate analgesia.⁷⁶ Dopaminergic activation in the VTA also enhances endogenous opioid release in the PAG, facilitating descending inhibition and attenuating nociceptive input at the spinal level. In parallel, positive emotional states have been observed to enhance parasympathetic vagal tone and decrease stress-induced sympathetic activity, thereby improving the body’s pain-inhibition capacity.^77,78 This aligns with neuroimaging evidence that feelings of happiness and joy are associated with increased functional connectivity between the ACC and PAG, suggesting a stronger activation of descending inhibitory pathways during CPM.⁷⁹

Even though positive emotions support the regulation of the aforementioned systems, their effects may be context-dependent. In a conditioned pain learning study, inducing positive affect via pleasant stimuli did not significantly reduce generalized avoidance or relief behaviors in response to pain cues in humans.⁸⁰ This suggests that while positive emotions can influence pain perception through descending inhibitory control, they may not override learned avoidance patterns reinforced through experience.

The Interplay Between Catastrophization, Negative Emotions, and Pain

Catastrophization and negative emotions share many overlapping mechanisms, reflecting their interrelated nature. The relationship between catastrophization and negative emotions is bidirectional. The trait model of catastrophization posits that individuals with greater negative affect are more prone to catastrophizing. Furthermore, depression can diminish self-efficacy and perception of coping abilities, two concepts highly implicated in the cognitive and coping models of catastrophization.^20,81 On the other hand, higher levels of catastrophization are associated with greater depressive symptoms, in part through repetitive negative thoughts and an adverse response to stress.^82,83

Experiencing pain can also contribute to negative emotions and future catastrophization. Greater pain intensity is associated with more mood disorders or anxious symptoms in a dose-dependent manner across several studies.^83–85 This may be due to the adverse impacts of pain that extend beyond the symptom itself. For example, sleep is something negatively impacted by pain, and poor sleep has been demonstrated to be a risk for depressive symptoms.^86,87 Regarding catastrophization, the cognitive model suggests that prior experiences impact future perceptions.²⁴ If prior experiences with pain were challenging, it is plausible that even seemingly minor instances of pain in the future may trigger catastrophization and contribute to a higher intensity of pain perceived.

Clinical Significance and Implications

With an understanding of mechanisms involved in catastrophization and emotions in relation to pain, there are several interventions that target specific pathways that extend beyond what is considered to be typical pain management strategies. Mindfulness exercises (ie., meditation) are widely available therapies that can be incorporated for potential benefits in parasympathetic activation and, to a lesser extent, reduction of sympathetic activity.⁸⁸ Mindfulness and relaxation exercises (eg., deep breathing) have also been shown to reduce HPA axis activation significantly.⁸⁹ Yoga is another low-cost and widely accessible exercise that has been associated with reductions in both sympathetic activity and HPA axis activation.⁹⁰ In addition to shifting adverse thought processes, cognitive behavioral therapy may also be implemented to reduce cortisol levels.^37,91 Mindfulness exercises and high-intensity interval training are modalities that have been implicated in enhancing endogenous opioid release, though this has been reported only in limited samples.^92,93 Additional general strategies include engaging in activities or social interactions that promote positive emotions, such as happiness and joy.

There are also measures that can be taken in the treatment workflow. As previously discussed, coping strategies and the tendency to catastrophize should be assessed early on so that early action can be taken to address maladaptive thought processes. Furthermore, the use of contextual factors can induce effects associated with enhanced endogenous opioid release and changes in brain regions involved in catastrophization, emotions, and pain (eg., dorsolateral prefrontal cortex).^94,95 Such contextual factors include better communication focused on positive outcomes and maintaining a patient-centered approach that values the patient’s input.

Future Directions

Despite extensive evidence linking catastrophization and emotions to increased pain intensity, key gaps remain in our understanding of this process. While current theories describe distinct mechanisms, catastrophization and emotions likely comprise dynamic interactions across systems. Future studies should aim to develop integrative frameworks that combine the cognitive, social, biological, and neural aspects into a unified model. The advent of machine learning tools and network-based modeling approaches could help researchers formalize these complex interactions.

Moreover, most existing studies rely on cross-sectional self-reports to measure catastrophization and assess emotions, which limits the understanding of long-term changes. Self-reports’ accuracy depends on the individual’s ability for introspection and recall, which may not accurately capture the process of catastrophization and the onset of emotions as they occur within the individual. Future research should move beyond this static metric toward person-centered, multimodal quantification strategies using data across timepoints. Quantitative measures of neural processes with fMRI and physiological markers of autonomic activation may provide more objective data to complement the existing self-report questionnaires. Higher-dimensional data, combined with clustering algorithms, can help elucidate patterns in individualized representations.

Overall, larger samples remain needed for stronger evidence and greater generalizability. Future studies should incorporate longitudinal designs, which are better suited to assessing the dynamic nature of catastrophization, emotions, and pain. These processes change throughout one’s lifetime across different contexts, and it would be of interest to observe what other mediating variables may be involved. Additional research is also needed to determine whether the results from experimental pain models can be translated to the chronic pain population. Integration of neuroimaging with behavioral measures would also be beneficial for a more complete understanding of the underlying processes. To facilitate the broader incorporation of psychosocial and lifestyle interventions, more translational research is needed to evaluate how these interventions alter the physiologic and neural mechanisms underlying catastrophization and emotions.

Conclusion

Catastrophization and negative emotions modulate pain through shared mechanisms of HPA axis overactivation, sympathetic overdrive, diminished endogenous opioid release, and weakened prefrontal cortex regulation. The main difference between the two is that catastrophization involves increased DMN connectivity, which contributes to negative self-referential thought processes. These mechanisms highlight the utility of psychosocial and lifestyle interventions, such as mindfulness exercises and cognitive-behavioral therapy.

Disclosure

Alaa Abd-Elsayed reports being a consultant for Medtronic, Curonix, Avanos and Averitas. The authors report no other conflicts of interest in this work.